Neurosurgery Jurnal

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ORI GINAL RES E ARCH Open Access

Monitoring of cerebral oxygen saturation duringresuscitation in out-of-hospital cardiac arrest: afeasibility study in a physician staffed emergencymedical systemJens-Christian Schewe , Marcus O Thudium* , Jochen Kappler, Folkert Steinhagen, Lars Eichhorn, Felix Erdfelder,Ulrich Heister and Richard Ellerkmann

AbstractBackground: Despite recent advances in resuscitation algorithms, neurological injury after cardiac arrest due tocerebral ischemia and reperfusion is one of the reasons for poor neurological outcome. There is currently noadequate means of measuring cerebral perfusion during cardiac arrest. It was the aim of this study to investigatethe feasibility of measuring near infrared spectroscopy (NIRS) as a potential surrogate parameter for cerebralperfusion in patients with out-of-hospital resuscitations in a physician-staffed emergency medical service.Methods: An emergency physician responding to out-of-hospital emergencies was equipped with a NONINcerebral oximetry device. Cerebral oximetry values (rSO 2 ) were continuously recorded during resuscitation andtransport. Feasibility was defined as >80% of total achieved recording time in relation to intended recording time.Results: 10 patients were prospectively enrolled. In 89.8% of total recording time, rSO 2 values could be recorded(213 minutes and 20 seconds), thus meeting feasibility criteria. 3 patients experienced return of spontaneouscirculation (ROSC). rSO2 during manual cardiopulmonary resuscitation (CPR) was lower in patients who did notexperience ROSC compared to the 3 patients with ROSC (31.6%, 7.4 versus 37.2% 17.0). ROSC was associatedwith an increase in rSO2 . Decrease of rSO2 indicated occurrence of re-arrest in 2 patients. In 2 patients a mechanicalchest compression device was used. rSO 2 values during mechanical compression were increased by 12.7% and19.1% compared to manual compression.Conclusions: NIRS monitoring is feasible during resuscitation of patients with out-of-hospital cardiac arrest and canbe a useful tool during resuscitation, leading to an earlier detection of ROSC and re-arrest. Higher initial rSO 2 valuesduring CPR seem to be associated with the occurrence of ROSC. The use of mechanical chest compression devicesmight result in higher rSO 2 . These findings need to be confirmed by larger studies.

Keywords: NIRS, CPR, Cerebral oximetry, Near infrared spectroscopy, Resuscitation, Mechanical chest compression

* Correspondence: [email protected] Equal contributorsDepartment of Anaesthesiology, University of Bonn Medical Center,Sigmund-Freud-Str. 25, 53105 Bonn, Germany

2014 Schewe et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the CreativeCommons Attribution License (http://creativecommons.org/licenses/by/4.0 ), which permits unrestricted use, distribution, andreproduction in any medium, provided the original work is properly credited. The Creative Commons Public DomainDedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article,unless otherwise stated.

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BackgroundSpontaneous circulation in out of hospital cardiac arrest(OHCA) may be restored in up to 50% of patients in thepresence of well-trained emergency physicians [ 1-4].Despite these promising results in the treatment of OHCA, survival rates remain low.

Discharge rates of 14% and 20% are reported in theseemergency medical systems (EMS) [ 4], and 1-year survival rates can reach up to 11% [2]. Outcome dependson professional EMS treatment including proper postresuscitation therapy and implementation of treatmentstrategies as published in current guidelines [ 5]. Lately,investigations revealed an improvement in neurologicaloutcome in patients treated with therapeutic hypothermiafollowing return of spontaneous circulation (ROSC) afterOHCA [ 6]. Multiple mechanisms are discussed to be re-sponsible for this neuroprotective effect [ 7]. Undoubtfully,

sufficient perfusion pressure during CPR is also crucial forneurological outcome. During basic life support chestcompressions (frequency and depth of compression) aswell as ventilation (end-expiratory CO 2 ) are poor mea-sures to evaluate the performance of adequate resusci-tation. During CPR, cerebral blood flow decreases to20-50% compared to normal values [ 8-10]. At the sametime, neurological outcome and survival depend on suf-ficient cerebral blood flow. To date, it is impossible toprovide helpful measurements to predict neurologicaloutcome during out-of-hospital resuscitation.

Regional cerebral oximetry with near infrared spec-

troscopy (NIRS) has emerged as a surrogate parametermonitoring cerebral perfusion in the intraoperative andintensive care setting [ 11]. The method uses the effectthat light in the near-infrared spectrum can penetratethe skull, thus allowing measurements of oxyhemoglo-bin. The absorption of light permits the measurement of oxyhemoglobin, desoxyhemoglobin, and total hemoglobin[12]. Ono et al. have revealed that decreasing intraoper-ative rSO2 values due to hypotension are associatedwith major morbidity and mortality after cardiac sur-gery [13]. Murkin et al. could show that intraoperativetreatment of low rSO 2 values resulted in decreasedmajor organ morbidity or mortality [ 14]. Small clinicalstudies have addressed the feasibility of NIRS technol-ogy in measuring cerebral oxygen saturation in patientsduring CPR. These studies included in-hospital re-suscitation [ 15-17], and out-of-hospital cardiac arrest[18,19], as well as a combination of the two [ 20,21].The authors suggest that the use of NIRS for cerebraloximetry is promising for monitoring patients withcardiac arrest. However, none of these studies focusedon routine use in a physician-staffed EMS. In summary,data is still limited, but available studies suggest thatNIRS monitoring can provide a real-time non-invasivemarker of cerebral perfusion and thus cerebral oximetry

may have a role in optimising cerebral perfusion in car-diac arrest.

The aim of this study was to investigate the feasibility of NIRS monitoring in out-of-hospital cardiac arrests ina physician-staffed emergency medical service in daily routine. Cerebral oximetry (rSO 2 ) was measured duringstandard cardiopulmonary resuscitation. This includedthe optional use of a mechanical chest compression device, a decision left to the discretion of the emergency physician.

MethodsSettingThe emergency medical service (EMS) of the City of Bonn serves 320,000 residents in a service area of 141 km 2 , with a population density of 2,250 persons/km 2 . The city reflects urban features. A total of 12 basic

life support (BLS) units and 3 advanced life support(ALS) units serve (2 of them 24 hours/7 days and 1 only 10 hours weekdays) in a two tier system. The EMS has84,240 BLS-unit hours/year and 19.410 ALS-unit hours/ year.

The EMS system responds to 33,600 emergency calls,increasing about 3-5% per year, with 26,000 BLS-unittransports and 7,600 ALS unit interventions per year. InBonn patients are admitted to 12 hospitals, all with dif-ferent care levels.

The BLS units are at least staffed with one emergency medical technician (EMT) and one paramedic. The ALS

units are staffed with one paramedic and one physician.Physicians on the ALS units are predominantly anaes-thesiologists and have passed at least 2 years of post-graduate training as well as a special emergency trainingcourse according to regulations of the German medicalacademy. The incidence of CPR in the EMS of Bonn iswithin 45 55 CPRs/100,000 inhabitants/year.

NIRS deviceThe NONIN EQUANOX Model 7600 regional oximetry system (Nonin Medical, Plymouth, Minnesota, USA) is aportable 4-wavelength cerebral oximeter. It weighs ap-proximately 900 grams, plus 180 grams for 2 sensorpods in the 2 sensor configuration. Dimensions are305108130 mm. Once the device is activated and asensor is attached, it displays continuous rSO 2 data inpercent from 0 to 100. Readings are sampled every 4 sec-onds. The monitor is equipped with a storage battery lasting for 4 hours when fully charged.

Study population/data acquisitionThe study was performed from October 2012 to July 2013. One ALS unit, which is on duty from Monday until Friday from 8 a.m.- 6 p.m., was equipped with theNIRS device. Prior to the beginning of the study, 3

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physicians were trained for half an hour in the use of the device according to legal requirements. Wheneverdispatched to emergencies with suspected cardiacarrest, which was the case when a lifeless person wasreported, the physician carried the NIRS device to thescene. All patients age >18 years with non-traumaticcardiac arrest were included. Exclusion criteria were:trauma, hypothermia 80%) of total achieved recording time in relation to intendedrecording time. Data is displayed as mean standarddeviation if not mentioned otherwise.

The study was approved by the local ethics committeeof the University of Bonn Medical Center.

ResultsTen consecutive patients (8 male and 2 female) were in-cluded. Mean age was 73 13 years ranging from 50 to90 years (see Table 1 for demographic data). Overall re-cording time was 237 minutes and 36 seconds. The oxim-etry signal was lost during 24 minutes and 16 seconds,resulting in 213 minutes and 20 seconds of clinical record-ing time during CPR. With 89.8% total recording time,feasibility criteria were met.

ROSC was achieved in 3 of 10 patients (30%). Figure 1displays data of a patient having not experienced ROSC.Initially 3 patients had ventricular fibrillation (VF) onarrival at the scene, while 7 patients were asystolic. Of the 3 patients with VF, 2 experienced ROSC. Of the 7

patients with initial asystole, 1 could be converted into ashockable rhythm and ROSC was established followingdefibrillation.

All 3 patients with ROSC were admitted to hospital.Of these patients, one (patient #1) was admitted to ICU after coronary intervention but eventually showed nosigns of neurological recovery. CT scans showed exten-sive brain damage, so that therapy was limited and thepatient died on ICU (see Figure 2 for NIRS data). Thesecond patient (patient #5) to experience ROSC was dis-charged after successful coronary intervention and ICU stay without neurological impairment (Cerebral Per-

formance Category, CPC 1, good performance). In thethird patient where ROSC was achieved despite initialasystole (patient #8), rSO 2 increased slowly after ROSCwas detected (Figure 3). After ROSC, spontaneous circu-lation could only be maintained under massive doses of vasopressors during transport into the hospital and thepatient died shortly after admission. 2 patients weretransported to a hospital with ongoing CPR with manual

Table 1 Demographic and NIRS data of all 10 included patientsPatient Age Gender Initial ECG rSO 2 during

manual CPR (%)rSO2 during mechanicalcompression (%)

rSO2 after ROSC (%) rSO2 after end of CPR (no ROSC, %)

1 64 VF 35.3 6.9 - 58.3 4.6 -2 77 Asy 35.4 3.0 - - 33.1 0.9

3 82 Asy 30.5 0.7 - - 30.9 0.3

4 90 Asy 35.6 1.7 - - 36.0 0.4

5 53 VF 45.7 5.3 - 63.2 8.0 -

6 76 Asy 38.0 5.9 - - 29.3 1.4

7 82 Asy 18.2 3.1 - - 20.4 0.5

8 74 Asy 30.5 1.3 - 35.3 4.2 -

9 50 VF 37.4 4.7 42.2 2.9 - -

10 84 Asy 21.3 2.5 25.4 2.3 - -

Data is presented in mean standard deviation. VF: ventricular fibrillation, Asy: asystole.



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as well as mechanical chest compressions (load distribut-ing band CPR, AutoPulse device, ZOLL, Chelmsford,MA, USA). In both cases, CPR attempts were terminatedin the emergency department of the admitting hospital,based on further examination and laboratory results by the hospital physicians. In 5 cases (50%), resuscitation wasunsuccessful and the patients died at the scene.

Mean rSO 2 under manual chest compression (n = 10)was 32.8% 8.1 compared to 29.9% 5.9 after termin-ation of chest compressions (n = 7) (relative decrease inrSO 2 of 8.7%). A mechanical chest compression devicewas used in 2 patients. Since battery capacity of the

device was limited and CPR had to be continued manu-ally, rSO2 readings during manual and mechanical chestcompression could be recorded. In one patient, mechan-ical compression led to a relative increase in rSO 2 of 12.7% (rSO2 42.2% vs. 37.4%). In the second patient rSO 2during mechanical compression was 19.1% higher com-pared to manual compression (rSO 2 25.3% vs. 21.3%, seeFigure 4).

In all patients with ROSC (n = 3), an increase in rSO 2was observed under spontaneous circulation. Mean rSO 2increased from 37.2% 7.7 before ROSC to 52.3% 14.9at time of ROSC, a relative increase of 40.6%.

Figure 1 NIRS data of patient #2 who never experienced ROSC.

Figure 2 NIRS data of patient #1 who had initial VF and experienced ROSC. After defibrillation and conversion into PEA there was anincrease in rSO2 before ROSC could be diagnosed. rSO 2 decreased again prior to re-arrest.



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Offline analysis showed that ROSC was indicated by an increase in rSO 2 well before the emergency physiciandiagnosed ROSC through a palpable pulse in 2 patients(Figure 2). In 1 patient with initial asystole rSO 2 in-creased after ROSC was diagnosed (Figure 3). In parallel,rSO 2 decreased before the emergency physisican decidedto restart CPR due to recurrent ventricular fibrillation in2 patients (see raw data of patient 1, Figure 2).

rSO 2 during CPR was lower in patients who did notexperience ROSC compared to the 3 patients with ROSC(31.6 7.4%, vs. 37.2 17.0%, see Figure 5).

DiscussionThis study demonstrated the feasibility of rSO 2 monitor-ing via NIRS during resuscitation in out-of-hospital car-diac arrest in a physician-staffed emergency medicalsystem, both at the scene and also during transport of patients. Feasibility criteria for monitoring rSO 2 weremet by the NIRS device, providing values in 89.8% of total recording time. Moreover, a concomitant detectionof increasing NIRS values in patients where ROSC wasobtained and a decrease of NIRS values following re-arrest with the onset of VT was observed.

Figure 3 NIRS data of patient #8 with ROSC after initial asystole. After ROSC rSO2 increased slowly while circulation could only be maintainedwith high doses of vasopressors.

Figure 4 NIRS data of patient #10 who never experienced ROSC. A mechanical chest compression device (load distributing band CPR) wasused for CPR. Due to limited battery capacity CPR had to be continued manually resulting in lower rSO 2 values.



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In a different study, Newman et al. reported no detect-able rSO 2 signal in patients with out-of-hospital cardiacarrest [ 18]. Contrary to these findings, we could record

stable values, possibly due to a general technological im-provement in modern NIRS devices.Only 1 out of 10 patients survived without neuro-

logical impairment (Cerebral Performance Category,CPC 1, good performance). This conforms with thegeneral resuscitation outcome of the EMS of the City of Bonn as reported in a larger study [ 4]. It is remarkablethat this patient had the highest rSO 2 readings duringCPR and ROSC (45.7% 5.27 and 63.2%, 8.02, respect-ively). However, this individual finding is too limited todraw conclusions on general neurological outcome andNIRS measurements during CPR.

Ahn et al. suggested a relationship between rSO 2 andROSC as well as a relationship between low rSO 2 andunsuccessful CPR [ 21] Koyama et al. drew similar con-clusions following their results [ 17]. Our results are con-sistent with these previous findings, observing lowerrSO 2 readings corresponding with futile resuscitation ef-forts compared to rSO 2 values in patients with success-ful CPR (rSO2 31.5% 7.1 vs. 37.2% 17.0, Figure 5).The second patient to experience ROSC survived morethan 24 hours, but ultimately suffered hypoxic braindamage. In this patient, ROSC was detected after a notableincrease in rSO 2 (35.3%, 6.94 during CPR vs. 58.3%, 4.63 after ROSC). However, before ROSC occurred, NIRS

readings showed a long period of low rSO 2 (Figure 2).One could speculate rSO 2 levels were low for too long andneurological damage was therefore irreversible. Unfortu-nately, NIRS monitoring was not continued after hospitaladmission. In future, the initial NIRS reading and thetrend during the initial phase of resuscitation might helpto predict outcome in terms of ROSC, survival and/orneurological outcome.

In the 2 patients mentioned above, rSO 2 decreasedbefore cardiac re-arrest was observed by the emergency physician. Frisch et al. published similar observations forperipheral tissue oximetry [ 19] and Meex et al. for cerebraloximetry [ 20]. We believe that NIRS could potentially im-prove CPR protocols by serving as an early-warning sys-tem detecting hemodynamic instability after ROSC priorto re-arrest.

In both of these patients, NIRS values increased rap-

idly with ROSC. In contrast, rSO 2 increased slowly afterROSC in patient 8 (see Figure 3). Vasopressors had to beused to sustain circulation during transportation untiltherapy was finally withdrawn in the emergency depart-ment. Our study is too limited to draw assumptionsbetween the dynamics of increase in NIRS followingROSC and stable versus unstable hemodynamics and thepossible underlying pathology.

Several studies have found an increase in rSO 2 afterROSC in patients [ 18-20]. Only Kmrainen et al.reported that rSO 2 increases prior to clinical detectionof ROSC [15]. It may be speculated that the time delay

between increase of rSO 2 in 2 cases of our study prior todocumented ROSC is due to delayed clinical detectionof ROSC by the physician. Guidelines recommend con-tinuous chest compression for 2 minutes after defibril-lation before analysis of cardiac rhythm and pulse.Nevertheless, within these two minutes, ROSC might bedetected by increasing rSO 2 . In future, it may be possibleto differentiate between sufficient and insufficient cere-bral perfusion as detected by a significant increase inNIRS guiding the physician to continue or interruptmanual chest compression.

The use of mechanical compression devices for CPRstill remains controversial. In previous studies, a higherarterial pressure and cardiac perfusion pressure were ob-tained with mechanical CPR devices versus manual chestcompression [ 22,23]. A recent meta-analysis by Westfallet al. suggests the superiority of mechanical devices versus manual chest compression regarding ROSC [ 24].However, there is insufficient evidence for the superior-ity of mechanical chest compression devices in terms of neurological outcome [ 25]. To our knowledge, we arethe first to provide data on NIRS monitoring duringmechanical and manual chest compression in OHCA.Kmrainen et al. could not show a significant increasein rSO 2 by improving CPR with a feedback device

Figure 5 Scatter plot and mean rSO 2 values during CPR of patients (n = 7) who never experienced ROSC and patients (n = 3)with ROSC.



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(improved quality of manual chest compression) [ 15].Whether this also applies to mechanical CPR deviceshas not been shown. In both patients where the devicewas applied, rSO 2 values were increased by 12% and 19%compared to manual compression. This finding couldsupport the theory that the use of mechanical CPRdevices can achieve higher cerebral perfusion pressurecompared to manual chest compression. However, wecannot rule out that increasing arterial CO 2 might haveinfluenced measured rSO 2 values based on autoregula-tion of cerebral blood flow influenced by changing arter-ial CO2 . The detected increase in measured rSO 2 valuesduring mechanical chest compressions could in theory also be explained by increasing arterial CO 2 [26].

During resuscitation, end-tidal CO 2 values are alsoused as a surrogate parameter for arterial CO 2 and thusas an indirect measurement of the achieved cardiac

output during CPR. End-tidal CO 2 during resuscitationis believed to be a quality marker of CPR performance[27]. In this study, end-tidal CO 2 values during resusci-tation were measured, but not recorded to the memory card due to technical reasons, and thus were not avail-able for offline analysis, which limits our observationalstudy.

ConclusionsCerebral oximetry using NIRS for out-of-hospital cardiacarrest is feasible in a physician-staffed EMS. rSO 2 moni-toring can help detect ROSC and hemodynamic instabil-

ities resulting in re-arrests. rSO 2 values measured duringapplication of a mechanical chest compression devicewere higher than during manual chest compression. Fur-ther investigations are needed to confirm whether theseresults can be explained by improved cerebral perfusion.

Competing interests The authors declare that they have no competing interests.

Authors contributionsJCS, MT, and RE designed the study. MT, JK, FS, LE, FE, and UH acquired andanalyzed data. MT and JCS drafted the article. All authors read and approvedthe final manuscript.

Acknowledgments

We thank the emergency physicians and the Fire Department of the City of Bonn for their continued support.

Received: 18 January 2014 Accepted: 29 September 2014

References1. Berdowski J, Berg RA, Tijssen JGP, Koster RW: Global incidences of out-of-

hospital cardiac arrest and survival rates: Systematic review of 67prospective studies. Resuscitation 2010, 81:1479 1487.

2. Fischer M, Fischer NJ, Schttler J: One-year survival after out-of-hospitalcardiac arrest in Bonn city: outcome report according to the Utsteinstyle . Resuscitation 1997, 33:233 243.

3. Herlitz J, Bahr J, Fischer M, Kuisma M, Lexow K, Thorgeirsson G:Resuscitation in Europe: a tale of five European regions. Resuscitation1999, 41:121 131.

4. Neukamm J, Grsner J-T, Schewe J-C, Breil M, Bahr J, Heister U, Wnent J,Bohn A, Heller G, Strickmann B, Fischer H, Kill C, Messelken M, Bein B,Lukas R, Meybohm P, Scholz J, Fischer M: The impact of response timereliability on CPR incidence and resuscitation success: a benchmark study from the German Resuscitation Registry. Crit Care Lond Engl 2011,15:R282.

5. Nolan JP, Soar J, Zideman DA, Biarent D, Bossaert LL, Deakin C, Koster RW,Wyllie J, Bttiger B, ERC Guidelines Writing Group: European ResuscitationCouncil Guidelines for Resuscitation 2010 Section 1: Executive summary.Resuscitation 2010, 2010(81):1219 1276.

6. Arrich J, Holzer M, Havel C, Mllner M, Herkner H: Hypothermia forneuroprotection in adults after cardiopulmonary resuscitation. CochraneDatabase Syst Rev 2012, 9:CD004128.

7. Chalkias A, Xanthos T: Post-cardiac arrest brain injury: pathophysiologyand treatment. J Neurol Sci 2012, 315:1 8.

8. Pernat A, Weil MH, Sun S, Tang W: Stroke volumes and end-tidal carbondioxide generated by precordial compression during ventricular fibrillation.Crit Care Med 2003, 31:1819 1823.

9. Bartlett RL, Stewart NJ Jr, Raymond J, Anstadt GL, Martin SD: Comparativestudy of three methods of resuscitation: closed-chest, open-chestmanual, and direct mechanical ventricular assistance. Ann Emerg Med 1984, 13(9 Pt 2):773 777.

10. Fischer M, Dahmen A, Standop J, Hagendorff A, Hoeft A, Krep H: Effects of hypertonic saline on myocardial blood flow in a porcine model of prolonged cardiac arrest. Resuscitation 2002, 54:269 280.

11. Ghosh A, Elwell C, Smith M: Review article: cerebral near-infraredspectroscopy in adults: a work in progress. Anesth Analg 2012,115:1373 1383.

12. Moerman A, Wouters P: Near-infrared spectroscopy (NIRS) monitoring incontemporary anesthesia and critical care. Acta Anaesthesiol Belg 2010,61:185 194.

13. Ono M, Brady K, Easley RB, Brown C, Kraut M, Gottesman RF, Hogue CW Jr:Duration and magnitude of blood pressure below cerebralautoregulation threshold during cardiopulmonary bypass is associatedwith major morbidity and operative mortality. J Thorac Cardiovasc Surg2014, 147:483 489.

14. Murkin JM, Adams SJ, Novick RJ, Quantz M, Bainbridge D, Iglesias I, ClelandA, Schaefer B, Irwin B, Fox S: Monitoring brain oxygen saturation duringcoronary bypass surgery: a randomized, prospective study. Anesth Analg2007, 104:51 58.

15. Kmrinen A, Sainio M, Olkkola KT, Huhtala H, Tenhunen J, Hoppu S:Quality controlled manual chest compressions and cerebral oxygenationduring in-hospital cardiac arrest. Resuscitation 2012, 83:138 142.

16. Ito N, Nanto S, Nagao K, Hatanaka T, Nishiyama K, Kai T: Regional cerebraloxygen saturation on hospital arrival is a potential novel predictor of neurological outcomes at hospital discharge in patients with out-of-hospital cardiac arrest. Resuscitation 2012, 83:46 50.

17. Koyama Y, Wada T, Lohman BD, Takamatsu Y, Matsumoto J, Fujitani S, TairaY: A new method to detect cerebral blood flow waveform in synchronywith chest compression by near-infrared spectroscopy during CPR. Am J Emerg Med 2013, 31:1504 1508.

18. Newman DH, Callaway CW, Greenwald IB, Freed J: Cerebral oximetry inout-of-hospital cardiac arrest: standard CPR rarely provides detectablehemoglobin-oxygen saturation to the frontal cortex. Resuscitation 2004,63:189 194.

19. Frisch A, Suffoletto BP, Frank R, Martin-Gill C, Menegazzi JJ: Potential utilityof near-infrared spectroscopy in out-of-hospital cardiac arrest: an illustrativecase series. Prehospital Emerg Care Off J Natl Assoc EMS Physicians Natl Assoc State EMS Dir 2012, 16:564 570.

20. Meex I, Deyne CD, Dens J, Scheyltjens S, Lathouwers K, Boer W, VundelinckxG, Heylen R, Jans F: Feasibility of absolute cerebral tissue oxygensaturation during cardiopulmonary resuscitation. Crit Care 2013, 17:R36.

21. Ahn A, Nasir A, Malik H, DOrazi F, Parnia S: A pilot study examining therole of regional cerebral oxygen saturation monitoring as a marker of return of spontaneous circulation in shockable (VF/VT) and non-shockable (PEA/Asystole) causes of cardiac arrest. Resuscitation 2013,84:1713 1716.

22. Duchateau F-X, Gueye P, Curac S, Tubach F, Broche C, Plaisance P, Payen D,Mantz J, Ricard-Hibon A: Effect of the AutoPulse automated band chestcompression device on hemodynamics in out-of-hospital cardiac arrestresuscitation. Intensive Care Med 2010, 36:1256 1260.



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23. Timerman S, Cardoso LF, Ramires JAF, Halperin H: Improved hemodynamicperformance with a novel chest compression device during treatment of in-hospital cardiac arrest. Resuscitation 2004, 61:273 280.

24. Westfall M, Krantz S, Mullin C, Kaufman C: Mechanical versus manual chestcompressions in Out-of-hospital cardiac arrest: a meta-analysis. Crit CareMed 2013, 41:1782 1798.

25. Ong MEH, Mackey KE, Zhang ZC, Tanaka H, Ma MH-M, Swor R, Shin SD:Mechanical CPR devices compared to manual CPR during out-of-hospitalcardiac arrest and ambulance transport: a systematic review. Scand J Trauma Resusc Emerg Med 2012, 20:39.

26. Kolb JC, Ainslie PN, Ide K, Poulin MJ: Effects of five consecutive nocturnalhypoxic exposures on the cerebrovascular responses to acute hypoxiaand hypercapnia in humans. J Appl Physiol Bethesda Md 1985 2004,96:1745 1754.

27. Morley PT: Monitoring the quality of cardiopulmonary resuscitation. Curr Opin Crit Care 2007, 13:261 267.

doi:10.1186/s13049-014-0058-yCite this article as: Schewe et al.: Monitoring of cerebral oxygensaturation during resuscitation in out-of-hospital cardiac arrest: afeasibility study in a physician staffed emergency medical system.Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine2014 22:58.

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